What is Fructositis?

Fructositis describes an episodic inflammatory lung condition triggered by consumption of foods and beverages with elevated levels of excess free fructose (EFF). The onset of symptoms is marked by a surge in airway mucus secretion associated with dry, unproductive cough; symptoms progress to chronic bronchitis, asthma, and lung inflammation. Fructositis is often associated with gas and abdominal discomfort, currently thought to be a result of fructose malabsorption.[3] Results of recent epidemiology research provide evidence of the association between EFF and asthma (see news and updates), but more research is needed to prove a causal association between regular excess free fructose intake and lung/ auto-immune diseases. More research must be done before the condition can become medically recognized.

Fructositis.org Mission

Raise awareness

about the link between HFCS, EFF and asthma, chronic bronchitis, auto-immune disease

Promote

the need for HFCS-free, EFF-free food labeling.

Fundraise

for research to learn more about the mechanisms involved and how to diagnose fructositis

Establish a forum

to share up-to-date facts and information about the disease

Campaign

for food labels that contain details of excess free fructose levels.

Fructositis in Context

A Silent Epidemic

The inability to adequately absorb excess free fructose is a medically recognized disease known as Fructose Malabsorption. Research indicates that it affects 10 - 30% or more of average adults, when fructose is consumed in high relative proportion to glucose as occurs in high fructose corn syrup, apple juice, and fruit drinks with a high apple juice content.[5][20-22] Limited research has been done to establish the precise prevalence of fructose malabsorption in children. Limited testing shows them to be at higher risk at lower levels of EFF consumption. Existing research suggests that more than 40% of children don't adequately absorb excess free fructose. Rates of malabsorption are thought to be highest among children under 4 years of age. The exact reasons why some people can adequately absorb excess free fructose whereas others cannot remains unknown.[9-10][20-22][54-55] Existing fructose malabsorption research suggests many people cannot adequately absorb excess free fructose at present levels of consumption. In 1996, the FDA reaffirmed HFCS as a Generally Recognized as Safe (GRAS) food, despite the findings of existing research. HFCS per capita consumption is now estimated at just under a pound a week. This is down from its 1999 peak of over a pound a week.

When challenged with 1 gram of fructose per kg of body weight, 25 of 57 (44%) children ages 0.1 to 6 years showed incomplete absorption. In children aged 1-3 years, incomplete absorption was significantly higher.[9][10]

The Link to Fructose Malabsorption

When fructose malabsorbers ingest more excess free fructose than their bodies can absorb, fructose concentrations increase in the digestive tract and may cause symptoms of abdominal and stomach pain, gas, bloating, and fatigue.[21-22][51-52] According to the recently proposed fructositis disease hypothesis, unabsorbed and highly reactive fructose may participate in the formation of immunogenic biomolecules in the digestive tract known as FruAGE. Once formed these biomolecules may gain access to the bloodstream. Chronic bronchitis and asthma are thought to result when FruAGE bind pro-inflammatory receptors[3] (RAGE) known to be highly concentrated in the lungs, inner ears, heart, lymph nodes, and connective tissues.[2] These receptors have been implicated in inflammation; mucus hypersecretion of the airways; bronchial hyper-responsiveness; tissue damage; aberrant repair; and airway constriction, obstruction, and remodeling which can eventuate in compromised lung function.[18] These receptors have been found to be elevated in a number of auto-immune conditions. This gives rise to the possibility that this condition is associated with other idiopathic auto-immune diseases including arthritis, psoriasis, chronic fatigue syndrome, and others.

In 1970, sugar [sucrose] was the most available and used U.S. sweetener. Since then, the American diet shifted to include more HFCS and less sugar.[35-37] This shift is significant both for the large percentages of fructose malabsorbers and for those with chronic respiratory disorders including asthma and chronic bronchitis that may be attributable to fructositis disease.

The Unexplained Dramatic Rise in Childhood Asthma

According to the Asthma and Allergy Foundation of America (AAFA), asthma prevalence increased among school children by 80 percent and among preschool children by 160 percent between the years of 1980 to 1994. In 2005, 8.9% of children in the United States had asthma. In 2007, 29% of children who had a food allergy also had asthma. A November 2007 report from the American Lung Association titled, Trends in Asthma Morbidity and Mortality, cites that an average of one out of every 10 school-aged child has asthma. [34]

This trend has affected black children much more significantly than children of other races and ethnicities. In 2009, according to a May 2011 Vital Signs Report from the Centers for Disease Control (CDC) and Prevention, about 1 in 6 (17%) of non-hispanic black children had asthma, the highest rate among racial/ ethnic groups. They cite the greatest rise in asthma rates was among black children (almost 50% increase) from 2001 through 2009.

These dramatic increases are not without consequences as asthma is the third-ranking cause of hospitalization among children under 15.[4] The current annual economic cost of asthma amounts to more than $56 billion annually.[34]

Rising Rates of Asthma Parallel Rising Rates of HFCS Consumption

An Interactive Timeline.

1959

Richard O. Marshall of the Corn Products Company (now Ingredion) files a patent for enzymatic conversion of glucose to fructose, making HFCS possible.

1960-1974

HFCS hits the U.S. market in 1967. By 1974, the average annual per capita consumption is 2.5 dry pounds per year. Death rates with asthma as the underlying cause of death decline by 66%, from 28.2 deaths per million in 1960 to 9.5 deaths per million in 1974. Prevalence data does not become available until 1980.

1975-1979

From 1975-1979, average annual per capita consumption of HFCS grows by 215% to 13.1 dry pounds per year, or about a quarter of a pound per person per week. For comparison, HFCS consumption levels peak in 1999 at 56.7 dry pounds per year, a 433% increase from 1979. The period from 1975 to 1978 marks the years with the lowest rates of death attributable to asthma on record, at 8.2 deaths per million.

1980-1994

In 1980 the CDC begins to track asthma prevalence rates. The estimated prevalence of self-reported-12 month or current asthma in 1980 is 3.1%. By 1980, per capita consumption of HFCS reaches 16.9 dry pounds per year, or about a third of a pound per person per week.

On February 8, 1983, the FDA publishes a document (48 FR 5716) that lists HFCS as "Generally Recognized As Safe (GRAS)" for use in food (21 CFR 182.1866). This same year researchers report data from studies of fructose malabsorption and report alarmingly high rates of fructose malabsorption in adults and children. Widespread use of HFCS continues despite these reports.

From 1980 to 1994, asthma rates jump by 160% in children aged 0-4 years, establishing this group as the most vulnerable to the disease. Asthma rates in school-aged children rise by 80%. These increases confound researchers who note marked improvements in air quality occuring during this period. They point to other unknown factors as triggers. By 1994, average annual HFCS consumption reaches 50 dry pounds per person, an increase of 195% from 1980 levels.

1995-1999

In 1996, the FDA reaffirms HFCS is generally recognized as safe (GRAS).

HFCS consumtion peaks in 1999 at 56.7 dry pounds per year.

The CDC stops tracking asthma prevalence rates from 1996-2000. Levels shown on the image above represent an extrapolation from the documented 1995 levels to those of 2001.

2000-2004

In 2000, researchers discover that there are separate and distinct pathways for absorption of fructose consumed in excess of glucose (as occurs with HFCS) versus fructose consumed in equal proportion to glucose as occurs during consumption of table sugar(sucrose). Excess fructose as occurs with HFCS is absorbed via GLUT5, whereas co-transport of equivalent amounts of fructose and glucose occurs via GLUT2. This physiological distinction is likely key to understanding why consumption of table sugar does not trigger symptoms of fructositis disease whereas consumption of fructose consumed in excess of glucose (as occurs with HFCS) does.

2005-2009

A 2005 University of Kansas study confirms earlier malabsorption research findings. Scientists found that over 50% of subjects in a 15 person study tested positive for fructose malabsorption and associated gastrointestinal distress. These results were observed with fructose consumption levels as low as 25 grams. At present rates of consumption estimated to be approximately 60 - 70 grams daily these findings are alarming. No large group studies have been conducted to date.

2010-Present

The USDA establishes new HFCS consumer-level loss estimates in January of 2011, and proposes their adoption retroactively for the entire data span (1970 to the most recent year in the series).

According to the ERS June 2012 Sugar and Sweeteners Outlook, "the loss estimate for refined sugar and corn sweeteners (including HFCS) increases substantially from 20% to 34%, while the estimates for honey and [other] edible syrups decreases from the 20% formerly used by the ERS to 15%." The rationale for these new and retroactive loss estimates are unclear. They effectively decrease per capita HFCS consumption data dating back forty years by increasing amounts for "loss".

Patient reports to doctors of the link between consumption of HFCS and incidence of auto-immune reactivity have failed to prompt research and remain medically unrecognized.

Hover over the dates above to learn more about HFCS consumption and asthma prevalence during that time period.

Rising Rates of Asthma Parallel Rising Rates of HFCS Consumption

This dramatic rise in asthma amongst children during the period from 1980 to 1994 that continues to present day, coincides with another trend occurring during this same time frame.

It is a parallel trend not typically discussed in the context of rising rates of asthma. According to the United States Department of Agriculture's (USDA) September 2008 report by Haley et al titled, Sugar and Sweeteners Outlook, the early 1980's also coincides with when the US food industry began a steady increase in their use of high fructose corn syrup (HFCS) as the preferred sweetener.[37]

According to the USDA, since 1985, the rise in sugar demand, although strong, has been moderate compared with the growth of corn sweeteners. In 1980, annual per capita consumption of HFCS was 16.9 pounds; by 1999 it had grown to 56.7 pounds. Thus by 1999 per capita consumption had grown by 235% from its 1980 levels. By 1999 Americans were consuming more than a pound per week of HFCS.

While the biochemical processes linking aero- allergens and asthma have been studied extensively and are well understood, the mechanisms that link excess free fructose to lung disease are poorly understood. Despite case report evidence linking episodes of chronic bronchitis and asthma to consumption of high fructose corn syrup, the disease remains medically unrecognized and unresearched.[3]

Research is needed

Between 1980 and 1994, average HFCS consumption climbed 196% to nearly a pound per person per week.